The prevalence of infective endocarditis after aortic valve replacement

AbstractReplacement valve endocarditis occurred in 3.7% of 2443 patients who underwent primary or redo aortic valve replacements at The Prince Charles Hospital between December 31, 1969, and January 1, 1992, based on a cross-sectional follow-up in 1992 which was 98.8% complete. Because some patients had re-replacements during the study period, a total of 2686 operations were considered for analysis. A variety of replacement devices were used, including 571 allografts (21%), 1152 xenografts (43%), and 880 mechanical valves (36%). Insertion of an allograft valve resulted in a constant risk of endocarditis which, by multivariable hazard function analysis, negated the effect of any early-phase risk factors ( p < 0.0001). With other replacement devices, the risk of infection peaked early after operation (9 weeks) and then gave way to a constant risk. Compared with the risk associated with allograft valves, constant risk was higher when the replacement device was a Carpentier-Edwards xenograft ( n = 1021, p = 0.02) and lower when a St. Jude Medical mechanical valve was used ( n = 505, p = 0.05). In nonallograft recipients, the presence of active preoperative endocarditis ( p < 0.0001) or a concomitant synthetic aortic root replacement ( p = 0.0006) increased the magnitude of the early peaking risk. Regardless of replacement device, constant risk was increased in patients with renal dysfunction ( p = 0.01), in younger patients ( p < 0.0001), and in those with active or healed preoperative endocarditis ( p = 0.04). When preoperative endocarditis was caused by Staphylococcus aureus, risk was higher than when it was caused by other organisms ( p = 0.04). A culture-positive postoperative wound infection was associated with increased risk of replacement valve infection ( p < 0.001) and when it occurred, the same organism was usually responsible (86%). Identification of patients at increased risk for replacement valve infection may lead to reduced morbidity through strategies such as selective use of replacement devices and antimicrobial prophylaxis. (J THORAC CARDIOVASC SURG 1995;110:1708-24